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首页> 外文期刊>Ukrainian Biochemical Journal >High thiamine dose restores levels of specific astroglial proteins in rat brain astrocytes affected by chronic ethanol consumption
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High thiamine dose restores levels of specific astroglial proteins in rat brain astrocytes affected by chronic ethanol consumption

机译：高硫胺素剂量可恢复受慢性乙醇消耗影响的大鼠脑星形胶质细胞中特定星形胶质蛋白的水平

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Long-term ethyl alcohol consumption induces a deficiency of essential nutrient thiamine (vitamin B1 ) and profoundly impairs metabolic processes in nervous tissue, resulting in structural and functional alterations in the central nervous system (CNS). This study was performed to evaluate protective effects of thiamine acute dose on the level of glial fibrillary acidic protein (GFAP), a sensitive marker of astroglia, and B1-related enzyme thiamine pyrophosphokinase (TPK) activity in brain of rats chronically exposed to ethanol. The rats were divided into three groups as follows: i) control group; ii) rats given 15% ethanol solution as drinking water for 9 months (EtOH group), iii) EtOH rats given thiamine per os in a dose of 2.0 mg/kg one day before experiment termination ( n = 4 in each group). GFAP levels were analyzed in cerebellum, brain cortex and hippocampus by western blot and immunohistochemistry. Brain TPK activity was measured with the use of the yeast apopyruvate decarboxylase apoenzyme (apoPDC). Thiamine concentration in liver was estimated with the use of thiochrome method. It was demonstrated that GFAP content was dramatically reduced in all studied brain regions of EtOH-exposed rats (approximately by 60%, P 1/sub liver level, however, had no effect on brain TPK activity. Our data suggest that thiamine deficit can play an important role in alcohol-induced damage to brain astroglia. It is emerged that high-dose thiamine administration can represent effective treatment option against chronic effects of ethanol impact on brain structures.
机译：长期饮酒会导致必需营养素硫胺素（维生素B1）的缺乏，并严重损害神经组织的代谢过程，导致中枢神经系统（CNS）的结构和功能发生变化。进行这项研究以评估硫胺素急性剂量对星形胶质细胞敏感标记神经胶质纤维酸性蛋白（GFAP）和B1相关酶硫胺素焦磷酸激酶（TPK）活性在长期暴露于乙醇的大鼠脑中的保护作用。将大鼠分成三组，如下：i）对照组; ii）给予15％乙醇溶液作为饮用水的大鼠，持续9个月（EtOH组），iii）终止实验的前一天，EtOH大鼠以os 2.0 / mg / kg的剂量口服硫胺素（每组n = 4）。通过蛋白质印迹和免疫组化分析小脑，大脑皮质和海马中的GFAP水平。脑TPK活性是通过使用酵母脱丙酮酸脱羧酶载脂酶（apoPDC）来测量的。肝脏中硫胺素的浓度用硫代色素法估算。结果表明，在所有研究过的EtOH暴露的大鼠脑区域中，GFAP含量均显着降低（约60％，P 1 肝水平对脑TPK活性没有影响。我们的数据表明，硫胺素缺乏症在酒精引起的脑星形胶质细胞损害中，α-内啡肽可能起重要作用，现已证明，大剂量硫胺素给药可代表有效的治疗选择，以应对乙醇对脑结构的慢性影响。

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